,UBE3A alleviates isoproterenol-induced cardiac hypertrophy through the inhibition of the TLR4/MMP-9

• 作 者: Yanfei Li Linlin Ma Sijie Gu Jiewen Tian Yilin Cao Zi Jin Jingyi Chen Bingbing Gu Jiayin Tu Zhixiao Wang Xinming Li Zhongping Ning Yueling Jin
• 机 构: Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Cardiovascular Departm
• 出 处: 生物化学与生物物理学报（英文版）
• 发表日期: 2020年1期
• 关键词: cardiac hypertrophy UBE3A TLR4 MMP-9

Cardiac hypertrophy is considered to be a leading factor in heart function-related deaths.In this study,we explored the potential mechanism underlying cardiac hypertrophy induced by isoproterenol.Our results showed that isoproterenol induced cardiac hypertrophy in AC16 cells,as reflected by the increased cell surface area and increased hypertrophic markers,which was accompanied by increased ubiquitin-protein ligase E3a (UBE3A) expression.Moreover,UBE3A knockdown by siRNAs accelerated cardiac hypertrophy,suggesting that increased UBE3A expression induced by isoproterenol might be a protective response and UBE3A might be a protective factor against cardiac hypertrophy.Our study also revealed that UBE3A knockdown increased the protein expression of the TLR4/MMP-9 pathway that has been shown to be associated with cardiac hypertrophy,which suggested that UBE3A-mediated protection is likely to be associated with the blockade of the TLR4/MMP-9 signaling pathway.UBE3A might be thus a potential target gene for the treatment of cardiac hypertrophy.